Dyslipidemia and Cardiovascular Risk in Obesity

Abstract

Obesity, in particular visceral obesity, has become a major worldwide health problem. Obesity increases cardiovascular risk through risk factors such as elevated fasting TG, high LDL cholesterol, low HDL cholesterol, elevated blood glucose and insulin levels, and high blood pressure. The typical dyslipidemia of obesity consists of increased TG and FFA, decreased HDL-C with HDL dysfunction, and normal or slightly increased LDL-C with increased small dense LDL. The concentrations of plasma apolipoprotein (apo) B are also often increased, partly due to the hepatic overproduction of apo B-containing lipoproteins. A delayed metabolism of intestinal-derived lipoproteins is usually seen in obesity. All lipoprotein abnormalities typically associated with visceral obesity in obesity carry an elevated pro-atherogenic potential. In particular, the prolonged presence in circulation of remnants of TG-rich lipoproteins and the preponderance of small dense LDLs are considered to play the most relevant role. Even though the reduction of LDL-C is the main target of treatment of dyslipidemia in obesity, apo B or non-HDL-C levels are recommended as secondary treatment targets. Treatment of dyslipidemia in obesity should be aimed at weight loss by increased exercise and improved dietary habits with a reduction in total calorie intake and reduced SFA intake. Medical therapy can be initiated if lifestyle changes are insufficient. Statins are the primary lipid-lowering drugs with effective reductions in LDL and remnant cholesterol levels. Moreover, the addition of fibrates may be considered in case of residual elevated TG and reduced HDL-C levels.